Lec1: Cardiovascular System= Heart and Blood Vessels
Blood Vessels
• Arteries: Carry oxygenated blood.
• Veins: Carry deoxygenated blood.
• Lymph: Contains lymphatic fluid and plays a role in immunity.
The Heart - 4 Chambers
Right Atrium (RA) Right Ventricle (RV)
Left Atrium (LA) Left Ventricle (LV)
Note: The Left Ventricle (LV) is stronger than the Right
Ventricle (RV) because it pumps blood throughout the body.
Heart Valves
• Tricuspid Valve: Between RA and RV.
• Mitral Valve: Between LA and LV.
• Aortic Valve: Between LV and the Aorta.
• Pulmonary Valve: Between RV and the Pulmonary Artery.
Note: The Mitral Valve and Aortic Valve are crucial for heart function.
Heart Layers
• Pericardium: Protects the heart, facilitates movement, and prevents
enlargement.
• Myocardium: The pumping muscle of the heart.
• Endocardium: Smooth inner lining that prevents clotting.
• Epicardium: Outer layer covering the heart surface.
Note: Pericardial fluid protects the heart, facilitates movement, and prevents excessive enlargement.
Aorta and Major Arteries
Ascending Aorta
1. Brachiocephalic Artery
2. Carotid Artery
3. Subclavian Artery
Descending Aorta
1. Thoracic Aorta
2. Abdominal Aorta
Blood Circulation
Pulmonary Circulation (minor)
• Starts from Right Ventricle (RV)
• Blood is sent to lungs via Pulmonary Artery
• Oxygenated blood returns to Left Atrium (LA) via
Pulmonary Veins
Note: Pulmonary Circulation starts in the Right Ventricle and ends in the Left Atrium.
Systemic Circulation
• Starts from Left Ventricle (LV)
• Blood is pumped into the Aorta
• Oxygen is delivered to tissues
• Deoxygenated blood returns to Right Atrium (RA) via Vena Cava
Note: Systemic Circulation starts in the Left Ventricle and ends in the Right Atrium.
Blood Vessels and Capillaries
• Arteries → Arterioles
• Capillaries
• Veins
Function of Capillaries:
• Deliver oxygen and nutrients to tissues.
• Remove carbon dioxide and waste via veins back to the heart.
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Heart Muscle
Myocardium (Cardiac Muscle): Responsible for pumping blood.
Pericardium:
• Outer part
• Inner part
• Filled with fluid to reduce friction and protect the heart.
Note: The Pericardium prevents excessive enlargement of the heart.
Electrical Conduction System of the Heart
Signal Transmission in the Heart
The electrical signal in the heart is transmitted simultaneously through:
• Intercalated Discs
• Gap Junctions
Why? This allows the heart to function as a single coordinated unit, ensuring synchronized contraction
of the atria and ventricles.
Types of Heart Muscles
Conductile (Conducting) Fibers:
• Multinucleated
• Contain Actin, Myosin, Tropomyosin,
and Troponin
• Generate and transmit electrical impulses
for heart contraction.
Intercalated Discs:
• Gap Junctions: Allow rapid transmission
of electrical impulses.
• Adhesion Membranes: Keep cells
connected during strong contractions.
Note: Intercalated discs allow all heart
muscle cells to contract simultaneously,
ensuring efficient pumping
Non-Conductile, Non-Contractile Cells:
• Do not participate in electrical conduction or contraction.
Cardiac Nucleus Characteristics
• Small, Condensed, and Rounded
Cardiac Conduction System
Sinoatrial (SA) Node
• Location: Right Atrium (RA)
• Position: Near the opening of the Superior Vena Cava.
• Function: Acts as the natural pacemaker, initiating the heartbeat.
Atrioventricular (AV) Node
• Location: Lower posterior region of the Right Atrium (RA).
• Function: Delays the electrical impulse to allow the atria to contract before the ventricles.
Atrioventricular (AV) Bundle (Bundle of His)
• Function: Transmits impulses from the AV node to the ventricles.
Purkinje Fibers
• Location: Walls of the ventricles.
• Function: Spread the electrical impulse rapidly, ensuring coordinated ventricular contraction.
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1
Lec 2 :Properties of the Heart
1. Conductivity ()
2. Auto-rhythmicity ()
3. Excitability ()
4. Contractility ()
Definition of Conductivity
The ability of cardiac muscle to transmit electrical impulses.
Why is the Sinoatrial Node (SAN) the Pacemaker of the Heart?
It is part of the nodal system and the fastest in generating impulses.
It suppresses other pacemaker activities.
It is the most dominant pacemaker of the heart.
Function of the Atrioventricular Node (AVN)
Allows time for Left Ventricular Filling (Diastole - ).
Allows time for Left Atrial Contraction (Systole - ).
Note: AVN is influenced by the Vagus nerve and the Autonomic Nervous System (Sympathetic &
Parasympathetic).
Contractility
Definition:
The ability of cardiac muscle to contract and then relax.
Mechanism of Muscle Contraction:
Action potential stimulates the muscle.
Opening of Long-lasting Calcium Channels (Ca²⁺).
Depolarized Ca²⁺ enters the cell (ECF → ICF).
Activator Ca²⁺ is released from the Sarcoplasmic
Reticulum.
Ca²⁺ binds with Troponin C.
Sliding of Actin over Myosin (Muscle contraction).
Leads to Contraction.
Note: Activator Ca²⁺ is essential for Depolarizing Ca²⁺. Strong relation between Contraction and Troponin C.
2
Relaxation (Diastole - )
Mechanism of Relaxation:
Ca²⁺ Reuptake by the Sarcoplasmic Reticulum.
Depolarized Ca²⁺ is expelled through Sarcolemmal Channels.
Na⁺/Ca²⁺ exchange restores ionic balance.
Note:
Ca²⁺ is removed from the cell via the Na⁺/Ca²⁺ Pump.
Additional Notes:
The strength of cardiac contraction depends on intracellular Ca²⁺ levels.
The heart muscle requires recovery time before the next contraction cycle.
Treatment of Tachycardia ():
Long-Lasting Calcium Channel Blockers reduce heart rate and excessive contractions.
Factors Affecting Contractility ()
Mechanical Factors
Preload :
The initial stretch of cardiac muscle fibers before contraction.
Depends on Venous Return (amount of blood returning to the heart).
Frank-Starling Law:
The greater the initial length of muscle fibers, the stronger the contraction (within physiological limits).
However! If blood returning exceeds 70ml, further stretching does not increase contractility.
2 Afterload
Occurs when there is increased resistance against LV ejection.
Causes of Increased Afterload:
Aortic Stenosis ():
Hypertension ().
Atherosclerosis ().
Chronic high afterload increases cardiac
workload.
High Afterload Risks:
Increased oxygen demand by the heart.
Leads to ventricular hypertrophy (heart
enlargement).
May cause heart failure in severe cases.
3
Cardiac Factors & Contractility
Increased cardiac mass can lead to ischemia, affecting Purkinje fibers and conduction.
Myocardial Infarction () results in muscle damage and reduced contractility.
Heart Rate & Contractility
Increased heart rate → Increased force of contraction.
Key Influences on Contractility:
Catecholamines (Epinephrine & Norepinephrine) → Stimulate calcium influx, increasing contractility.
Hypercalcemia (High Ca²⁺) → Stronger and prolonged contractions.
Role of Calcium in Cardiac Contraction
Calcium enters cardiac cells via action potentials.
Excess calcium prevents proper relaxation → Leads to sustained contractions.
Sympathetic stimulation increases calcium availability, enhancing contractility.
Effects of pH, CO₂, and Electrolytes on Contractility
Acidosis (↓ pH, ↑ H⁺ & CO₂) → Decreases contractility due to enzyme inhibition.
Alkalosis (↑ pH, ↓ H⁺ & CO₂) → Increases contractility but may cause arrhythmias.
Potassium (K⁺) & Contractility:
Hyperkalemia (High K⁺) → Weak contractions, risk of cardiac arrest.
Hypokalemia (Low K⁺) → Increases excitability, leading to arrhythmias.
Effects of Oxygen & Carbon Dioxide on Contractility
Increased O₂ → Enhances contractility.
Decreased O₂ (Hypoxia) → Weakens contractions, leading to heart failure.
CO₂ Retention (Hypercapnia) → Increases acidity, impairing myocardial contractility.
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Calcium Imbalance & Its Effects on the Heart
Hypercalcemia (Excess Ca²⁺):
Leads to sustained systole (constant contraction).
Can cause arrhythmias and increased cardiac workload.
Hypocalcemia (Low Ca²⁺):
Leads to weak contractions and heart failure.
Treatment: IV Calcium, but must be given cautiously!
Afterload & Its Effect on the Heart
Afterload = Resistance the heart must overcome to pump blood.
Causes of Increased Afterload:
Aortic Stenosis → Narrowing of the Aortic Valve.
Hypertension → Increased resistance in the Aorta.
Arterial Stiffness (Atherosclerosis) → Cholesterol buildup.
Aging & Rheumatic Fever → Valvular damage.
High Afterload Risks:
Increased oxygen demand.
Leads to ventricular hypertrophy (enlarged heart).
May result in heart failure.
Summary:
Contractility depends on calcium, pH, oxygen, CO₂, potassium, and autonomic stimulation.
The AMP Cycle increases contractility by stimulating calcium influx.
CO₂ retention & acidosis impair contractility, while alkalosis may cause arrhythmias.
Potassium imbalances (Hyperkalemia or Hypokalemia) can cause severe cardiac dysfunction.
Increased afterload leads to hypertrophy and heart failure risk.
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Lec 3:
2
Lec 4: Excitability & Automaticity
1-Excitability
The ability of cardiac muscle to respond to electrical impulses from SAN
( )
Mainly in the left ventricle
SAN (Sinoatrial Node)
The natural pacemaker of the heart
Generates impulses to regulate heartbeat
Time between impulses ≈ 0.8 sec
Phases of Excitability:
1. Absolute Refractory Period (ARP) → No excitability (Zero)
(
) (Systole +0.5Diastole)
2. Relative Refractory Period (RRP) → Partial excitability
(After Systole +0.5Diastole) (
)
Extra Systole (Abnormal Beat) ( )
Extra Systole = Abnormal impulse from an ectopic focus ( )
Caused by impulses from an abnormal pacemaker (not SAN)
Types of Extra Systole
Atrial Extra Systole Nodal Extra Systole Ventricular Extra Systole
Atrial Extra Systole
Less common because atria are less sensitive to abnormal impulses
Can be triggered by: Stress, Electrolyte imbalance, Overstimulation
Impulse originates from the atria but not from SAN
Nodal Extra Systole
Occurs during RRP ( RRP)
May become uncontrolled if impulse originates from AVN instead of SAN
( AVN
SAN)
Ventricular Extra Systole
Pathological condition! ( !)
Caused by: Ischemia, Infarction, Electrolyte disturbances
Dangerous because it affects cardiac output & may lead to:
Ventricular Tachycardia (VT) → Fast heartbeat
Ventricular Fibrillation (VF) → Life-threatening!
Cause: (Compensatory Pause & Impulse Disruption)
A compensatory pause occurs due to electrical impulse disruption (
)
SAN generates an impulse, but at the same time, another impulse is triggered in the left
ventricle
This leads to asynchronous contractions → Poor blood pumping → Risk of cardiac arrest!
( ، )
2-Automaticity
The ability of cardiac muscle to generate impulses automatically
(
)
Present in both SAN & ventricles
Time interval between impulses ≈ 0.75 - 0.8 sec (
0.75 - 0.8 )
AP of SAN (Action Potential of SAN)
Controls the natural heart rhythm ( )
Fast repolarization → Rapid impulse generation (
)
Factors Affecting Membrane Potential Stability
• K⁺ Outflux → Affects repolarization ( )
• Ca²⁺ Influx → Controls depolarization (
)
Ca+Channels
T-type Calcium Channels → Responsible for fast electrical current in SAN
( )
Transient Channels → Help regulate cardiac electrical impulses
( ).
1
Autonomic Control of the Heart
• The heart is controlled by the Autonomic Nervous System (ANS).
• The Sinoatrial Node (SAN) is responsible for generating heart impulses spontaneously.
• However, the ANS modifies the SAN rate depending on body needs.
SAN Rate: 100-120 bpm
Key Point:
The SAN naturally fires at 100-120 beats per minute (bpm), but under normal conditions, the
parasympathetic nervous system slows it down.
Effect of Autonomic Nervous System on the Heart
Sympathetic Nervous System → Increases SAN activity → Increases heart rate (up to 140 bpm).
Parasympathetic Nervous System → Decreases SAN activity → Decreases heart rate (to 70-80 bpm).
Key Point:
The sympathetic system prepares the body for activity ("fight or flight"), while the parasympathetic
system keeps it relaxed ("rest and digest").
Cardiac Control Centers in the Brainstem
Located in the Medulla Oblongata (part of the brainstem).
Cardioinhibitory Center (CIC) → Slows down heart rate
via the Vagus Nerve (CN X).
Vasomotor Center:
• (A) Cardioaccelerator Center (CAC) → Increases heart rate & contraction force (sympathetic control).
• (B) Vasodilatation Center (VDC) → Causes vasodilation (parasympathetic control).
عيرس حرش(Medulla Oblongata)
• CIC →
(Vagus nerve).
• CAC →
sympathetic
• VDC → .
2
Vagal Tone
• In resting conditions, the Vagus Nerve (CN X) dominates , leading to a decrease in SAN rate
(Parasympathetic effect).
• This is part of a Reflex Mechanism that helps maintain heart rate at a normal resting level.
:
(Vagus Nerve) SAN.
Key Point:
The Vagus Nerve is constantly inhibiting the SAN, preventing the heart from beating too fast at rest.
Important Question: Components of Vagal Tone?
Components of Vagal Tone
Receptor: Baroreceptor (pressure-sensitive receptor in blood vessels).
Afferent Nerve:
• Carotid Nerve → Branch of Glossopharyngeal Nerve (CN IX).
• Aortic Nerve → Branch of Vagus Nerve (CN X).
Central Control: Cardioinhibitory Center (CIC) in the Medulla Oblongata.
Efferent Nerve: Vagus Nerve (CN X) → Inhibits SAN and reduces heart rate.
Effect: SAN inhibition → Heart rate (70-80 bpm).
:
Vagus Nerve :
(Baroreceptors).
9+10.
CIC.
Vagus Nerve SAN.
bpm.
Key Point:
This mechanism prevents excessive heart rate increase and keeps the heart working efficiently.
3
Vagal Escape Phenomenon
• If excessive vagal stimulation occurs, and SAN is completely suppressed, the ventricles "escape"
the vagal effect and begin generating their own impulses.
• Right vagus nerve → affects SAN.
• Left vagus nerve → affects AVN.
:
Vagus Nerve
Vagal Escape.
• SAN
ventricles.
Key Point:
The heart has a backup system to ensure it keeps beating even if the primary pacemakers fail.
Complete Heart Block (Life-Threatening Condition)
• If both SAN and AVN are inhibited, the ventricles take over but at a very slow rate (16-40 bpm).
• This can lead to serious conditions, including:
o Arrhythmias (irregular heartbeats).
o Ventricular asystole (complete cessation of ventricular contractions).
o Complete Heart Block (total electrical conduction failure in the heart).
Key Point:
The Vagal Escape Phenomenon is life-saving in elderly patients with Complete Heart Block, as it ensures
the heart continues beating, even at a slow rate.
:
Complete Heart Block SAN AVN ventricles
.
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Cardiac Output (CO)
Definition:
The amount of blood pumped by each ventricle per minute.
Equation:
CO = Stroke Volume (SV) × Heart Rate (HR)
Example Calculation:
CO=70×70=4900CO = 70 \times 70 = 4900 ml/min
.
Factors Affecting CO
1. Heart Rate
Normal range: 60 - 100 bpm
Effect on CO:
Increases → CO decreases
Decreases → CO decreases
( bpm) CO !
Diastole Stroke Volume.
2. Stroke Volume (SV)
SV :
• Contractility
• Preload
• Afterload
If SV increases → CO increases
If SV decreases → CO decreases
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3. Venous Return
Definition: The amount of blood returning to the heart.
Factors Affecting VR
1. Blood Volume
Increases → VR increases
Decreases → VR decreases
2. Venous Valves
3. Venoconstriction
↑ Venoconstriction → ↑ VR
↑ Venodilation → ↓ VR
4. Skeletal Muscle Pump
5. Respiratory Pump
6. Gravity
→ ↓ VR
→ ↑ VR
